The purpose of this thesis was to examine the interaction between cardiovascular risk factors (particularly novel inflammatory measures) and short-term changes in physical activity. This is important as it is necessary to establish whether the changes that occur to these markers over the longer-term might be a consequence of short-term changes in physical activity. Chapter 4 investigated the challenges in handling the large volume of minute-by-minute data obtained from the use of a novel device for estimating physical activity energy expenditure from synchronous heart rate and accelerometer data. This chapter describes the development of specific software to enable efficient data-processing and evaluated the advantages and disadvantages of this new method of physical activity measurement. Chapter 5 sought to understand the reproducibility of various measures that were central to progress in this field in order to justify their inclusion in future intervention-based studies. This work showed that the inflammatory markers C-Reactive Protein and interleukin-6 and the lipid markers total cholesterol, high-density lipoprotein, low-density lipoprotein and triglycerides were all reproducible measures. The measurement of physical activity energy expenditure, when demarked into common categories, was also mostly reproducible. The circulating marker oxidised-low-density lipoprotein, an in-house adhesion assay and in-house mononuclear cell cytokine secretion assay were determined to be not reproducible and were not used further in this thesis. In Chapter 6 a group of highly active middle-aged men undertook one week of detraining where all structured exercise was removed but activities of daily living were allowed. It was shown that this short-term period of detraining did not elicit any changes in any of the inflammatory, lipid or glucose/insulin markers measured including a commercial, externally-validated whole-blood cytokine secretion assay. In Chapter 7 a sedentary group of middle-aged men performed daily brisk walking for 30 minutes over one week. This period of training did not elicit any change in any of the inflammatory, lipid or glucose/insulin markers measured; including no changes in glucose measures with an oral glucose tolerance test either one day after the last training session or three days later. The differences between the highly-active (Chapter 6) and sedentary (Chapter 7) participants in inflammatory markers were large with substantially higher concentrations for C-Reactive Protein and interleukin-6 in the sedentary middle-aged men. Because these do not change in response to relatively short-term detraining (Chapter 6) or training (Chapter 7) it appears that these differences represent long-term changes and adaptations. Therefore, in addition to being reproducible, fasting inflammatory and lipid markers are very stable with no changes after positive or negative short-term alterations in physical activity level. One immediate implication of this stability is improved ease of follow-up measures after interventions (e.g., training studies) since differences appear to reflect chronic changes in response to the regular training/detraining undertaken and not to recent exercise per se. In the future it will be important to establish better demarcations of acceptable physical activity behaviour. It will also be important to establish whether recently-trained individuals also exhibit stability in their inflammatory markers after a short-period of detraining and whether sedentary individuals are ever capable of achieving the blood profiles of their highly-active counterparts.